Resolving the fibrotic niche of human liver cirrhosis at single-cell level
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Abstract
Liver cirrhosis is a major cause of death worldwide and is characterized by extensive fibrosis. There are currently no effective antifibrotic therapies available. To obtain a better understanding of the cellular and molecular mechanisms involved in disease pathogenesis and enable the discovery of therapeutic targets, here we profile the transcriptomes of more than 100,000 single human cells, yielding molecular definitions for non-parenchymal cell types that are found in healthy and cirrhotic human liver. We identify a scar-associated TREM2+CD9+ subpopulation of macrophages, which expands in liver fibrosis, differentiates from circulating monocytes and is pro-fibrogenic. We also define ACKR1+ and PLVAP+ endothelial cells that expand in cirrhosis, are topographically restricted to the fibrotic niche and enhance the transmigration of leucocytes. Multi-lineage modelling of ligand and receptor interactions between the scar-associated macrophages, endothelial cells and PDGFRα+ collagen-producing mesenchymal cells reveals intra-scar activity of several pro-fibrogenic pathways including TNFRSF12A, PDGFR and NOTCH signalling. Our work dissects unanticipated aspects of the cellular and molecular basis of human organ fibrosis at a single-cell level, and provides a conceptual framework for the discovery of rational therapeutic targets in liver cirrhosis.
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In published single-cell RNA-sequencing datasets from MASH patient livers, FOXP3+ cells expressing canonical Treg transcripts such as IL2RA, CTLA4, and TNFRSF18 are present.
“Focusing our analysis on the CD4+ T cell compartment, we identified FOXP3+ cells expressing canonical Treg cell transcripts, including IL2RA, CTLA4 and TNFRSF18 (Fig. 1D, right panel).”
From Regulatory T cells safeguard liver health during metabolic-associated steatohepatitis (2026) · cites this paper as [22]
Extended Data Figure 3 describes single-cell analysis of liver T cells from five healthy and five cirrhotic donors, so the paper provides a relevant T-cell dataset. It does not report FOXP3+ cells coexpressing IL2RA, CTLA4 and TNFRSF18. Its NASH analysis in Extended Data Figure 7 uses whole-liver microarray data, not a NASH-specific single-cell T-cell dataset. (LLM, conf=0.84)
Experimental — accuracy not yet measuredLAMs are equivalent to scar-associated macrophages (SAM) in human MASH.
“are equivalent to the scar-associated macrophages (SAM) in human MASH (6–8)”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
The Results section ('Pro-fibrogenic phenotype of scar-associated macrophages'; page unavailable) reports expansion of scar-associated macrophages (SAMΦ) in patients with NASH, now termed MASH. Our copy does not identify these cells as LAMs or establish that the two populations are equivalent. (LLM, conf=0.86)
Experimental — accuracy not yet measuredConditioned media from TREM2+ SAM were reported to be more fibrogenic compared to their TREM2− non-scar-associated counterparts.
“However, conditioned media from TREM2+ SAM were reported to be more fibrogenic compared to their TREM2− non-scar-associated counterparts (6).”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
The Results section (‘Distinct macrophage subpopulations inhabit the fibrotic niche’; page unavailable) reports that conditioned media from TREM2+CD9+ scar-associated macrophages promoted fibrillar collagen expression in human hepatic stellate cells. Extended Data Figure 10c describes tests with media from other macrophage populations, but the available text does not report that the scar-associated macrophage media was more fibrogenic than media from TREM2− counterparts. (LLM, conf=0.86)
Experimental — accuracy not yet measuredGpnmb, Cd9, and Fabp5 are characteristics of SAM described in humans.
“that are characteristics of SAM described in humans (6, 7).”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
The Results section, “Distinct macrophage subpopulations inhabit the fibrotic niche” (page unavailable), identifies CD9 as a marker of scar-associated macrophages in human livers. Searches of our copy for GPNMB and FABP5 found no passages identifying either as a characteristic of those cells, so the three-gene claim is only partly supported. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSingle-cell transcriptomics has revealed the presence of numerous subsets/states of macrophages in any given injured tissue in humans.
“The growing accessibility of single-cell transcriptomics has also revealed the presence of numerous subsets/states of macrophages in any given injured tissue in humans (30–33).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
The Results section, “Distinct macrophage subpopulations inhabit the fibrotic niche,” identifies several macrophage clusters in human cirrhotic liver, including scar-associated macrophages and Kupffer cells. This supports the liver example, but this paper alone does not establish that numerous macrophage states occur in any given injured human tissue. (LLM, conf=0.87)
Experimental — accuracy not yet measured
During active fibrogenesis, the macrophage pool is dominated by pro-inflammatory and pro-fibrogenic macrophages.
“While the precise roles of the different subsets generated during injury and resolution are still under investigation, the prevailing dogma is that during active fibrogenesis, the macrophage pool is dominated by pro-inflammatory and pro-fibrogenic macrophages (31, 89, 90).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
In Results, “Distinct macrophage subpopulations inhabit the fibrotic niche” reports that scar-associated macrophages expand in cirrhotic livers and promote collagen expression. “Pro-fibrogenic phenotype of scar-associated macrophages” identifies pro-fibrogenic genes, including IL1B and CXCL8. Neither section establishes that pro-inflammatory and pro-fibrogenic macrophages dominate the overall macrophage pool during active fibrogenesis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMacrophages in the fibrotic liver called LAMs, SAMs, and NAMs in different studies largely share a conserved transcriptional profile.
“A good example of this is the population of macrophages in the fibrotic liver, which have been called LAMs, SAMs, and NAMs in different studies, despite largely sharing a conserved transcriptional profile (31, 104, 108).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
The Results sections ‘Distinct macrophage subpopulations inhabit the fibrotic niche’ and ‘Pro-fibrogenic phenotype of scar-associated macrophages’ identify scar-associated macrophages (SAMΦ) in fibrotic liver and describe their defining gene-expression signatures (page numbers unavailable). Our copy does not compare SAMΦ with populations called LAMs or NAMs, so it does not establish that all three largely share a conserved transcriptional profile. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLAMs produce mediators such as SPP1 and TGF-β that activate HSCs and may promote fibrogenesis.
“these cells also produce mediators such as SPP1 and TGF-β that activate HSCs and hence may promote fibrogenesis (31).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
The Results sections on scar-associated macrophages report SPP1 expression and show that macrophage-conditioned media promotes fibrillar collagen expression in human HSCs, supporting a potential pro-fibrogenic effect. The cited passages do not identify TGF-β as a mediator produced by these macrophages or show that SPP1 itself activates HSCs. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredLAMs, SAMs and NAMs exhibit a very similar transcriptional profile, with the precise name reflecting the different studies in which these cells were identified.
“Notably, these cells exhibit a very similar transcriptional profile, with the precise name (LAM, SAM, or NAM) reflecting the different studies in which these cells were identified.”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
The Results section, “Pro-fibrogenic phenotype of scar-associated macrophages” (page unavailable), defines a transcriptional signature for scar-associated macrophages (SAMΦ). Our copy does not compare SAMΦ with LAMs or NAMs or say that the three names reflect the studies in which the cells were identified. (LLM, conf=0.83)
Experimental — accuracy not yet measuredSingle-cell RNA-seq studies have identified, in human MASLD, macrophage subsets largely analogous to those previously described in mouse.
“Single-cell RNA-seq studies conducted by independent groups have identified, in human MASLD, macrophage subsets largely analogous to those previously described in mouse (196–198). These include resident KCs (VSIG4+/CD163+/MARCO+/TIMD4+), Mo-KCs (VSIG4+/CD163+/MARCO-/TIMD4-), LAMs (VSIG4-/TREM2+/CD9+) and C-LAMs (VSIG4-/CX3CR1+/CCR2+).”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [198]
The Results ('Pro-fibrogenic phenotype of scar-associated macrophages'; page unavailable) report that human and mouse TREM2+CD9+ scar-associated macrophages cluster together in a cross-species single-cell analysis. But the human single-cell samples were from cirrhotic livers; the paper assessed NAFLD/NASH using microarray deconvolution and biopsy staining, not single-cell RNA-seq of human MASLD. It therefore supports the cross-species analogy for one macrophage population, but not the claim as framed for human MASLD. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSub-populations of macrophages and HSCs in the healthy human liver have been described in single-cell data.
“While sub-populations of macrophages and HSCs in the healthy human liver have been described in single-cell data10–12, these subpopulations, and potential gene expression variations within, have not been resolved within the lobule organization at single-cell resolution in the human liver.”
From Spatial transcriptomics of healthy and fibrotic human liver at single-cell resolution (2025) · cites this paper as [11]
The Results section on macrophages identifies distinct Kupffer-cell clusters in human liver samples that included healthy livers, supporting the macrophage portion. The Results section on mesenchymal cells identifies one cluster as hepatic stellate cells and distinguishes it from other mesenchymal populations, but does not describe multiple HSC subpopulations in healthy human liver. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSAMs localize around fibrotic scars.
“and fibrotic scars (SAM) (6)”
From Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2 (2024) · cites this paper as [6]
Monocytes recruited to zones of steatosis and fibrosis appear to take on an alternative profile, which has been given multiple names, including lipid-associated macrophages (LAMs), scar-associated macrophages (SAMs) and NASH-associated macrophages (NAMs).
“On the other hand, those monocytes recruited to zones of steatosis and fibrosis appear to take on an alternative profile, which has been given multiple names, including lipid-associated macrophages (LAMs), scar-associated macrophages (SAMs) and NASH-associated macrophages (NAMs) (31, 104, 108, 109).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [31]
Recent single-cell human liver studies have largely focused on chronic liver disease rather than ALF, with emphasis on non-parenchymal cell populations.
“Recent single-cell human liver studies have largely focused on chronic liver disease rather than ALF, with emphasis on non-parenchymal cell populations7–9”
From Multimodal decoding of human liver regeneration (2024) · cites this paper as [7]
TREM2+/CD9+ macrophages exhibit a pro-fibrogenic phenotype and accumulate within collagen-rich fibrotic niches in cirrhotic livers.
“Notably, TREM2+/CD9+ macrophages have been shown to exhibit a pro-fibrogenic phenotype and to accumulate within collagen-rich fibrotic niches in cirrhotic livers, leading to their designation as scar associated macrophages (SAMs) (198).”
From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [198]
The role of TREM2 in regulating the pro-fibrotic AM phenotype in lung fibrosis remains unclear.
“except for the mere recognition as a marker of fibrosis-associated macrophages39,43–45, the role of TREM2 in regulating the pro-fibrotic AM phenotype in lung fibrosis remains unclear.”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [39]
In liver, a TREM2+CD9+ subset of macrophages that differentiate from circulating monocytes expands during liver cirrhosis and contributes to fibrosis.
“In the liver, a TREM2+CD9+ subset of macrophages that differentiate from circulating monocytes expands during liver cirrhosis and contributes to fibrosis (Ramachandran et al., 2019).”
From TREM2 Modulation Remodels the Tumor Myeloid Landscape Enhancing Anti-PD-1 Immunotherapy (2020) · cites this paper as Ramachandran et al., 2019
Both macrophage populations were identified by expression of CD74, while Mac 2 cells also expressed CD5L and MARCO, most consistent with non-inflammatory macrophages or Kupffer cells.
“Both macrophage populations were identified by expression of CD74, while Mac 2 cells also expressed CD5L and MARCO (Fig. 2d, i; Supplementary Fig. 6b), most consistent with non-inflammatory macrophages or Kupffer cells10,11,21.”
From Spatial transcriptomics of healthy and fibrotic human liver at single-cell resolution (2025) · cites this paper as [11]
In human single-cell RNA-sequencing datasets, Treg frequency is significantly higher in MASH livers than in control livers.
“Notably, the Treg frequency was significantly elevated in MASH livers relative to that of controls (Fig. 1E), echoing the Treg enrichment observed in the CDAHFD and AMLN models.”
From Regulatory T cells safeguard liver health during metabolic-associated steatohepatitis (2026) · cites this paper as [22]
Extended Data Figure 3 compares T-cell and innate lymphoid-cell fractions in healthy versus cirrhotic livers, but the available text does not report a significant increase in Tregs in MASH livers. Extended Data Figure 7 examines NASH liver samples, but its frequency analysis concerns scar-associated macrophages, not Tregs. Searches for Treg and regulatory T cells found no passage establishing the claimed comparison. (LLM, conf=0.76)
Experimental — accuracy not yet measuredPDGFRB expression was concentrated along the edges of ALDOB-expressing hepatocytes in a distribution expected for HSCs, which are located in the subendothelial space.
“PDGFRB expression was concentrated along the edges of ALDOB-expressing hepatocytes in a distribution expected for HSCs, which are located in the subendothelial space11 (Supplementary Fig. 2a–f).”
From Spatial transcriptomics of healthy and fibrotic human liver at single-cell resolution (2025) · cites this paper as [11]
The citation is attached to the statement that hepatic stellate cells occupy the subendothelial space. The Results section on mesenchymal cells identifies an HSC population by RGS5 staining, but our copy does not state its subendothelial location. Searches for “subendothelial” and “space of Disse” found no passage establishing that location; the PDGFRB–ALDOB staining is attributed to the citing paper’s supplementary figure. (LLM, conf=0.70)
Experimental — accuracy not yet measuredIn cirrhosis-enriched neighbourhoods, Milo recovered over-expression of known markers of scar-associated endothelium, including ACKR1 and PLVAP.
“In the cirrhosis-enriched neighbourhoods, we recovered over-expression of known markers of scar-associated endothelium, including ACKR1 and PLVAP (Fig 5F) [2].”
From Differential abundance testing on single-cell data using k-nearest neighbor graphs (2022) · cites this paper as [2]
This study revealed the presence of two disease-associated endothelial cell populations in the fibrotic niche, characterized as CD34+PLVAP+VWA1+ and CD34+PLVAP+ACKR1+ populations.
“In addition to providing a first-of-its-kind liver cell atlas, this study revealed the presence of two disease-associated endothelial cell populations in the fibrotic niche, characterized as CD34+PLVAP+VWA1+ and CD34+PLVAP+ACKR1+ populations.”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [335]
This same study identified PDGFRA as a marker of scar-associated fibroblasts in cirrhotic livers.
“Moreover, this same study identified PDGFRA as a marker of scar-associated fibroblasts in cirrhotic livers.”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [335]
One landmark study described the fibrotic niche in healthy and cirrhotic human livers via single-cell RNA sequencing.
“One landmark study described the fibrotic niche in healthy and cirrhotic human livers via single-cell RNA sequencing [335].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [335]
ScRNAseq of human cirrhotic livers has identified a subset of TREM2+CD9+ macrophages enriched in heavily scarred regions that secrete cytokines and growth factors, including EGF and PDGF-BB, to create a pro-fibrogenic niche for activated HSCs.
“ScRNAseq of human cirrhotic livers has identified a subset of TREM2+CD9+ macrophages enriched in heavily scarred regions of the liver that secrete cytokines and growth factors, including epidermal growth factor (EGF) and platelet-derived growth factor BB (PDGF-BB) to create a pro-fibrogenic niche for aHSCs (56).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [56]
This LAM population associates closely with activated HSCs and likely overlaps with scar-associated TREM2+ CD9+ macrophages described in human cirrhosis.
“This population was found to associate closely with aHSCs and likely overlaps with the scar-associated TREM2+ CD9+ macrophages described by Ramachandran et al. in scRNAseq of human cirrhosis (20, 56).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [56]
Fibrogenic TREM2+CD9+ scar-associated macrophages have been characterized in human cirrhosis.
“Separately, fibrogenic TREM2+CD9+ “scar-associated” macrophages have been characterized in human cirrhosis (56).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [56]
In silico trajectory analysis, based on spliced vs. unspliced mRNA ratios, suggested that TREM2+/CD9+ scar-associated macrophages were derived from blood monocytes.
“In silico trajectory analysis, based on spliced vs. unspliced mRNA ratios, suggested that these cells were derived from blood monocytes.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Immunofluorescence staining demonstrated that TREM2+/CD9+ macrophages were highly enriched in the fibrotic niche.
“Immunofluorescence staining demonstrated that these TREM2+/CD9+ macrophages were highly enriched in the fibrotic niche.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Ramachandran et al. used scRNAseq to identify a disease-associated TREM2+/CD9+ macrophage population that was significantly expanded in human cirrhotic livers.
“Ramachandran et al. used scRNAseq technology to identify a disease-associated TREM2+/CD9+ macrophage population that was significantly expanded in human cirrhotic livers.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Ligand-receptor pairs were localised to the fibrotic niche between scar-associated macrophages expressing TNFSF12 and PDGFB with myofibroblast receptors TNFSF12A and PDGFRA, respectively.
“Ligand-receptor pairs were localised to the fibrotic niche between scar-associated macrophages expressing TNFSF12 and PDGFB with myofibroblast receptors TNFSF12A and PDGFRA, respectively.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Gene ontology of the top differentially expressed genes in scar-associated macrophages identified pro-fibrogenic factors such as IL-1B, TREM2, CXCR4, CCR2, CXCL8, TNFSF12 and VEGFA, which regulate scar-producing myofibroblasts, upregulate inflammation and promote angiogenesis.
“Gene ontology of the top differentially expressed genes identified pro-fibrogenic factors, such as IL-1B, TREM2 (triggering receptor expressed on myeloid cells 2), CXCR4, C-C motif chemokine receptor (CCR)2, CXCL8, TNFSF12 and vascular endothelial growth factor (VEGF)A, which regulate scar-producing myofibroblasts, upregulate inflammation and promote angiogenesis.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Analysis of the transcriptome of scar-associated macrophages demonstrated a phenotype analogous to TREM2+/CD9+ BMDMs in mice.
“Analysis of the transcriptome of these scar-associated macrophages demonstrated a phenotype analogous to TREM2+/CD9+ BMDMs in mice.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Cognate, pro-fibrotic myofibroblast receptors were also identified for secreted phosphoprotein 1 and IL1β.
“Cognate, pro-fibrotic myofibroblast receptors were also identified for secreted phosphoprotein 1 and IL1β.75”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Ramachandran et al. identified a distinct population of scar-associated mesenchymal cells in the human liver expressing high levels of fibrogenic genes and the myofibroblast marker PDGFRA, topographically restricted to fibrotic septae, with pro-fibrogenic pathways including TNFRSF12A, PDGFR and Notch paired to ligands in scar-associated macrophages and scar-associated endothelia.
“Ramachandran et al. used this approach to identify a distinct population of scar-associated mesenchymal cells in the human liver expressing high levels of fibrogenic genes and the myofibroblast marker, PDGFRA. These myofibroblasts were topographically restricted to fibrotic septae and ligand-receptor analysis revealed a number of pro-fibrogenic pathways including TNFRSF12A, PDGFR and Notch. These”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Scar-associated LSECs expand in human cirrhosis, have a PLVAP+ and ACKR1+ transcriptome, and demonstrate pro-inflammatory ligand-receptor interactions such as TGFB1-TGFBR3, JAG1-NOTCH1 and CCL2-ACKR1.
“Scar-associated LSECs have been shown by scRNAseq to expand in human cirrhosis. These cells have a PLVAP+ and ACKR1+ transcriptome and demonstrate a number of pro-inflammatory ligand-receptor interactions, such as TGFB1-TGFBR3, JAG1-NOTCH1 and CCL2-ACKR1.75”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [75]
Seminal work from the Henderson group first profiled hepatic cells, including HSCs from fibrotic mouse and patient livers, and this has since been expanded to MASH by several groups including ours.
“Seminal work from the Henderson group first profiled hepatic cells, including HSCs from fibrotic mouse and patient livers (50, 51), which has since been expanded to MASH by several other groups including ours.”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [51]
LAMs are identified by TREM2, CD9, and SPP1 expression, which also mark scar-associated macrophages in cirrhotic patients, suggesting a common macrophage lineage across liver injury models.
“LAMs are identified by the expression of TREM2, Tetraspanin CD9 (CD9), and SPP1, which also represent markers of scar-associated macrophages (SAMs) in cirrhotic patients, suggesting a common macrophage lineage in different liver injury models (51).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [51]
Animal models implicate HSCs and immune cells, especially macrophages, as major cellular drivers of extracellular matrix turnover, through reduced secretion of ECM components and crosslinking enzymes and increased secretion of proteases and their inhibitors.
“Animal models implicate HSCs and immune cells, especially macrophages, as major cellular drivers of extracellular matrix turnover, both through reduced secretion of ECM components and crosslinking enzymes as well as increased secretion of proteases and their inhibitors (51, 52, 64, 262, 270-274).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [51]
Mature and plasma B-cell clusters have been detected by scRNAseq within areas of scarring in fibrotic livers of patients with cirrhosis.
“Mature and plasma B‐cell clusters have been also detected by sc‐RNAseq within areas of scarring in fibrotic livers of patients with cirrhosis.( 58 )”
From The Emerging Role of B Cells in the Pathogenesis of NAFLD (2021) · cites this paper as [58]
While many discoveries are based on mouse models, scRNA-seq analyses from human livers have identified SAMs as a unique population located in the fibrotic niche of cirrhotic livers of different disease aetiologies.
“While many of these discoveries have been based on mouse models, scRNA-seq analyses from human livers have also identified SAMs as a unique population located in the fibrotic niche of cirrhotic livers of different disease aetiologies.74”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [74]
Significant diversity and functional heterogeneity exist within the fibroblast population during organ fibrosis.
“Increasingly sophisticated experimental approaches have allowed discovery of significant diversity and functional heterogeneity within the fibroblast population during organ fibrosis22–25 .”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [22]
In the gastrointestinal tract, a single-cell census of the colonic mesenchyme revealed four fibroblast subsets in addition to pericytes and myofibroblasts, and identified a fibroblast subpopulation near the colonic crypt niche that expresses SOX6, F3, and WNT genes essential for colonic epithelial stem cell function.
“a single-cell census of the colonic mesenchyme revealed four subsets of fibroblasts in addition to pericytes and myofibroblasts, and identification of a fibroblast subpopulation proximal to the colonic crypt niche which expressed SOX6, F3 (CD142), and WNT genes essential for colonic epithelial stem cell function.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [22]
In colitis, the colonic crypt niche becomes dysregulated with the emergence of an activated mesenchymal population expressing TNFSF14, fibroblastic reticular cell-associated genes, IL-33, and lysyl oxidases, which leads to impaired epithelial proliferation and maturation.
“In colitis, this niche became dysregulated with emergence of an activated mesenchymal population expressing TNFSF14, fibroblastic reticular cell-associated genes, interleukin (IL)-33, and lysyl oxidases (LOX) leading to impaired epithelial proliferation and maturation”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [22]
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TREM-2 plays a protective role in cholestasis by acting as a negative regulator of inflammation
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- Authors
- Ramachandran, P., Dobie, R., Wilson-Kanamori, J. R., Dora, E. F., Henderson, B. E. P., Luu, N. T., Portman, J. R., Matchett, K. P., Brice, M., Marwick, J. A., Taylor, R. S., Efremova, M., Vento-Tormo, R., Carragher, N. O., Kendall, T. J., Fallowfield, J. A., Harrison, E. M., Mole, D. J., Wigmore, S. J., Newsome, P. N., Weston, C. J., Iredale, J. P., Tacke, F., Pollard, J. W., Ponting, C. P., Marioni, J. C., Teichmann, S. A., & Henderson, N. C.
- Affiliations
- Centre for Inflammation Research (GB)
- University Hospitals Birmingham NHS Foundation Trust (GB)
- Edinburgh Cancer Research (GB)
- Wellcome Sanger Institute (GB)
- Edinburgh Royal Infirmary (GB)
- National Institute for Health and Care Research (GB)
- Charité – Universitätsmedizin Berlin (DE)
- Albert Einstein College of Medicine (US)
- Institute of Genetics and Cancer (GB)
- European Bioinformatics Institute (GB)
- Corresponding author
- Ramachandran, P.
- Henderson, N. C.
- ORCID
- Ramachandran, P.
- Dobie, R.
- Henderson, B. E. P.
- Luu, N. T.
- Portman, J. R.
- Matchett, K. P.
- Brice, M.
- Taylor, R. S.
- Efremova, M.
- Carragher, N. O.
- Kendall, T. J.
- Fallowfield, J. A.
- Harrison, E. M.
- Mole, D. J.
- Wigmore, S. J.
- Newsome, P. N.
- Weston, C. J.
- Iredale, J. P.
- Tacke, F.
- Pollard, J. W.
- Ponting, C. P.
- Marioni, J. C.
- Teichmann, S. A.
- Henderson, N. C.
- Venue
- Nature
- Published
- 2019-10-09
- Volume
- 575
- Issue
- 7783
- Pages
- 512-518
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC6876711
- OpenAlex
- W2979595830
- Cited by
- 1,784
- References
- 98
- Citations by year
- 2026: 306 · 2025: 319 · 2024: 293 · 2023: 286 · 2022: 220 · 2021: 221 · 2020: 131 · 2019: 7
- FWCI
- 92.30
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Nature (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Apollo
- Funders
- Wellcome Trust (RE/18/5/34216, 103749, 101067/Z/13/Z, WT206194, 103749/Z/14/Z)
- University Hospitals Birmingham NHS Foundation Trust
- NIHR Bristol Biomedical Research Centre
- Cancer Research UK (22231)
- National Institute for Health and Care Research
- British Heart Foundation (RM/17/3/33381, RE/18/5/34216)
- Department of Health and Social Care
- Children's Liver Disease Foundation
- Tenovus
- University of Birmingham
- University of Bristol
- Medical Research Council (RM/17/3/33381, MC_PC_15049, MR/N008340/1, 103749, MC_PC_15075, MR/P008887/1, MC_UU_00007/15, MC_PC_15041, RE/18/5/34216, MR/N022556/1)
- Biotechnology and Biological Sciences Research Council (BB/N018869/1, RE/18/5/34216)
- Birmingham Biomedical Research Centre
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- liver cirrhosis, liver fibrosis, fibrotic niche, monocyte differentiation, collagen synthesis, TNFRSF12A, Notch signaling, non-parenchymal cells
- MeSH terms
- Animals, Duffy Blood-Group System, Female, Humans, Liver, Liver Cirrhosis, Macrophages, Male, Membrane Glycoproteins, Membrane Proteins, Phenotype, Receptors, Cell Surface, Receptors, Immunologic, Case-Control Studies, Cell Lineage, Receptor, Platelet-Derived Growth Factor alpha, Hepatocytes, Endothelial Cells, Mice, Hepatic Stellate Cells, Transendothelial and Transepithelial Migration, Single-Cell Analysis, Transcriptome, Tetraspanin 29
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